PC612 Mod 5 Cardiovascular
Terms in this set (241)
What are the cardiovascular drug classes?
Drugs-diuretics, Ace Inhibitors
ARBs, Calcium Channel Blockers, Beta Blockers, Vasodilators, Alpha Blockers
Coagulation Modifiers Agents
What are the etiologies of hypertension?
Excess body weight,
Excess dietary sodium
Reduced physical activity
Inadequate fruit, veggie and potassium intake
Excess alcohol consumption
What target organs are damaged by hypertension?
Heart: left ventricular hypertrophy, angina or MI, heart failure.
Brain: stroke or TIA
Kidney: chronic kidney disease
Other: Peripheral artery disease and retinopathy
What are some lifestyle modifications to reduce hypertension?
Reduction of 10 kg in weight can result in decrease of 5-20mmHg in systolic BP.
Dash diet=8-14 mmHg
Low sodium diet= 2-8
Physical activity= 4-9
Moderation ETOH= 2-4.
Weight reduction is highest, and smoking.
What impact does weight reduction have on hypertension?
Weight reduction is the lifestyle modification that has the most significant effect on hypertension. For every 10kg of weight loss, there is a 5-20 mmHg reduction in SBP.
What is the impact of a 5 mmHg reduction in BP?
Overall reduction in incidence: stroke 14%, CHD 9%, and all cause of mortality 7%.
What are the three types of hypertension?
1) White coat HTN
2) Secondary HTN
3) Essential HTN
What are the causes of secondary hypertension?
Renal artery stenosis-kidney disease
Pre-HTN Defined= SBP 120-139, DBP 80-89
Blood pressure above 115/75, CVD risk doubles with each increase of 20/10 mmHg.
Requires health-promoting lifestyle modificatons & patient involvement is key.
What should be the first recommended treatment for HTN?
When lifestyle modification fails, what are indicators to initiate drug therapy for HTN?
Not at goal BP (<140/90 mmHg or or <130/80 for those with diabetes or chronic kidney disease.)
Define Stage 1 HTN.
Systolic 140-159 or diastolic 90-99
What is the initial drug therapy for Stage 1 HTN?
Thiazide-Type Diuretics for most.
May consider ACE Inhibitor, ARB, Beta Blocker, Calcium Channel Blocker, or a combination.
Define Stage 2 HTN.
Systolic greater than 160 or diastolic greater than 100
What is the initial drug therapy for Stage 2 HTN?
Two drug combination for most. (Usually a Thiazide-Type Diuretic and ACE Inhibitor or ARB or Beta Blocker or Calcium Channel Blocker.) One of the two should be a diuretic or ACE/ARB.
What are considerations for refractory hypertension?
Patient adherence, volume overload, excess sodium intake, drug-induced, NSAIDS, sympathomimetics, black licorice, oral contraceptives, dietary supplements (ephedra, ma haung, bitter orange), obesity, and excess alcohol intake.
What are some botanicals that elevate blood pressure?
Black licorice (not botanical)
Which hypertensive agents impact the sympathetic nervous system (MOA)?
Calcium Channel Blockers
Centrally acting drugs
Which hypertensive agents impact vascular tone (MOA)?
Which hypertensive agents impact vascular volume (MOA)?
Angiotensin converting ensyme inhibitors (ACEIs) Angiotensin receptor blockers (ARBs)
Which medication should be included in initial drug therapy for most people?
At what point should you initiate anti-hypertenisve therapy with two agents?
When blood pressure is >20/10 mmHg above goal.
Most patients require 2 or more drugs to achieve goal BP.
Which cardiovascular drug class is recommended for all high-risk conditions with compelling indicator (HF, post-MI, high CAD risk, diabetes, CKD, stroke)?
An ACE inhibitor is indicated in any one of these categories and choosing a drug from this class is almost always going to be correct.
Diuretics are specifically indicated to treat what?
Heart failure, systolic hypertrophy, and the elderly.
Beta blockers are specifically indicated to treat what?
Ischemic heart disease, heart failure, tachyarrhythmia and essential tremor.
Calcium antagonists are indicated for what?
Isolated systolic hypertrophy, the elderly, and ischemic heart disease.
ACE inhibitors are indicated to treat for what?
Heart failure, post-acute MI, nephropathy diabetes type 1 and 2, and stroke.
ARA-II are indicated to treat what?
Nephropathy diabetes type 2, left ventriculary hypertrophy and intolerance to ACE inhibitors
Alpha blockers are indicated for what?
What is the site of action and MOA of diuretics?
The site of action is different locations of the renal tubule. Mechanism of action is increased urinary sodium and water excretion, which decreases extracellular fluid and/or plasma volume.
What effect do diuretics have on the cardiovascular system?
Acute decrease in cardiac output.
Chronic decrease in TPR and normal cardiac output.
What are the different types of diuretics?
Loop diuretics- furosemide, bumetadine.
K sparing- amiloride, spironolactone, triamterene.
Osmotic- mannitol; urea
What is the MOA of thiazide diuretics?
Reduce reabsorption of sodium and chloride in ascending loop of Henle & early distal tubules.
Increase K and bicarb excretion, decrease calcium excretion, and increase uric acid retention.
May benefit those who have osteopenia (decreased calcium excretion; loop diuretics have opposite effect).
What are side effects and contraindications of thiazide diuretics?
Side effects: hypokalemia, dehydration, hyperuricemia and IMPAIRED GLUCOSE TOLERANCE.
Contraindications: Gout due to increased uric acid, renal failure, and may worsen diabetes because of impaired glucose tolerance.
What are the indications for loop diuretics?
Indicated for edema with heart failure, cirrhosis and renal disease, and they are used when there is increased need for diuresis.
What is the MOA of loop diuretics?
Decrease sodium chloride reabsorption in the ascending loop of Henle & work in proximal & distal tubules.
Increase K excretion, decrease Ca and Mag reabsorption.
Efficacy is dose dependent.
No diuresis is seen in very low doses.
What are two common loop diuretics?
furosemide (Lasix) and bumetadine (Bumex)
What is it essential to check when combining a loop diuretic with digoxin? What is usually prescribed in conjunction with a loop diuretic?
Check potassium level.
Potassium is typically prescribed with a loop diuretic.
What are the side effects of loop diuretics?
MOST SIGNIFICANT is Hypokalemia; replace potassium!
What is the MOA of beta blockers?
Compete with adrenergic receptor binding sites.
Beta 1 receptors predominate in cardiac tissue; cardioselective!
Beta 2 receptors predominate in the bronchial & vascular smooth muscles & liver.
Decrease cardiac output by decreasing the rate, contractility and conduction velocity of the heart.
May decrease sympathetic activity & ventricular remodeling; used in stable heart failure patients.
What are the side effects of beta blockers?
BRADYCARDIA, postural hypotension, fatigue, dizziness, and sexual dysfunction. May worsen depression.
Worsens asthma: blocking of beta receptors may cause bronchial constriction. Selective beta 1 have less risk (preferred), they mainly affect the heart: metoprolol & atenolol. Noncardio selective: propranolol, nadolol.
What are some precautions with use of beta blockers?
Never stop abruptly, should always be tapered or get rebound hypertension.
May mask effects of hypoglycemia & inhibit glycogenolysis, therefore not recommended for diabetes.
Not recommended in heart block, COPD, asthma, bradycardia or severe heart failure.
Avoid with PVD.
Caution with exercise enthusiasts.
Which beta2 adrenergic agonist is prescribed for control of premature labor?
Terbutaline has selective action on beta 2 receptors & was used as a drug to delay preterm labor.
FYI: due to side effects of this drug which resulted in a Black Box warning, MgS04 is currently the preferred drug for preterm labor.
Explain how peripheral alpha 1 blockers work and give example.
Selective blockage of alpha-1 receptors peripherally resulting in vasodilation.
This action decreases peripheral resistance & venous return.
End in "azosin", ie prazosin (Minipress)
Positive benefits: Slight ↓ in T. Chol & LDL. Also reduce size of prostate so will see this drug given to older men.
What are the adverse effects and contraindications of alpha 1 blockers?
Adverse effects: orthostatic hypotension, palpitations, Bradycardia, and Edema
Contraindications: cardiovascular disease,
concomitant use of selective phosphodiesterase type 5 (PDE5) inhibitors, ie. tadalafil(Cialis) & vardenafil (Levitra)
What is the MOA of ACE inhibitors?
Prevent the conversion of angiotensin I to angiotensin II in the kidney, which prevents vasoconstriction of renal vessels.
Decrease degradation of bradykinin & increase synthesis of vasodilating prostaglandins.
Effects on HTN: vasodilation of renal vessels, potentiate water & sodium loss, & spare potassium.
Good choice for patients with diabetes (slows progression of renal failure) and HF.
End in "-pril" (i.e. enalapril [Vasotec]).
Work well with thiazides. Less effect with african americans...use CCB
What effects do ACE inhibitors have on hypertension?
Effects on HTN are vasodilation of renal vessels. It potentiates water & sodium loss, spares K+.
A good choice for patients with diabetes because it slows progression of renal disease & heart failure.
What are the side effects and contraindications in ACE inhibitors?
Side effects: Nonproductive cough & angioedema.
Contraindications: Do NOT give to patients taking K sparing diuretics, renal artery stenosis and in PREGNANCY TERATOGENIC EFFECTS.
NSAIDS can reduce the effects of ACE inhibitors, avoid use in patients on ACEs.
What is the MOA of angiotensin II receptor blockers (ARBs)?
Causes vasoconstriction & aldosterone secretion causing increase in sodium and water retention and activation of the sympathetic nervous system.
OFten come as a combo drug with HCTZ.
End in "sartan" (i.e. losartan [Cozar]).
Used when ACEs are not tolerated (i.e. cough).
Less effect with African americans...use CCB
What are the two groups of calcium channel blockers and what is their MOA?
DHPs: dihydropyridines (DHPs) and non-DHPs.
They relax arterial smooth muscle and depress cardiac contractility.
What are DHPs? What is their MOA?
Calcium channel blockers (dihydropyridines or "pines") i.e. amlodipine (Norvasc)
They have little effect on cardiac contractility. They are potent peripheral vasodilators which blunts negative inotropic effect. May cause reflex tachycardia due to peripheral vasodilation.
What are non-DHPs? What is their MOA? What particular indication have they been used for?
Calcium channel blockers (non-dihydropyridines) i.e. diltiazem and verapamil.
They decrease conduction rate at the SA node and slow AV conduction.
They have been used to decrease arrhythmias like SVT and A fib
What are precautions with use of calcium channel blockers?
CAN CAUSE REFLEX TACHYCARDIA (use beta blocker in combination to control this).
Causes peripheral edema, primarily in lower extremities.
Are not to be used with patients who are in heart block. Contribute to acid reflux as they inhibit contraction of LES.
Multiple drug-drug interactions.
What is the MOA of central alpha 2 receptor agonists? Precautions? Examples?
They stimulate alpha 2 adrenergic receptors in the brain resulting in decreased cardiac output, decreased sympathetic outflow, and decreased peripheral resistance.
Cause fluid retention so use with a diuretic.
Cause rebound HTN if stopped abruptly.
Examples: clonidine (Catapres), methyldopa (Aldomet), guanabenz (Wytensin), and guanfacine (Tenex)
What cardiovascular changes take place in pregnancy?
Increased stroke volume, increased heart rate, increased oxygen consumption, decreased SBP & DBP due to increased levels of estrogen and prostaglandins which cause vasodilation.
Decrease typically is during the first 24 weeks (20-24) of pregnancy.
What is the drug of choice for controlling blood pressure in pregnancy? Why? What is a reasonable alternative?
Methyldopa - Aldomet.
Best documented maternal and fetal safety record.
Does not alter maternal cardiac output or blood flow to uterus or kidneys.
Labetalol, a beta adrenergic receptor blocker, is a peripheral vasodilator and a reasonable alternative.
Why should antihypertensive dosage and response be closely monitored during pregnancy?
The blood pressure decreases during the first half of pregnancy.
Hyperlipidemia is a risk factor for what? What antilipemic drug can reduce MI risk, stroke, and death and by how much?
Significant risk factor for cardiovascular disease
Significant risk factor for strokes
In patients with diabetes, CAD or other occlusive arterial disease simvastatin use at 40mg/day reduced MI risk, stroke and death by 25%
What are the major classes of antilipemic agents?
HMG-CoA reductase inhibitors (statins)
Bile acid sequestrants/resins
Fibric acid derivatives
Cholesterol absorption inhibitors
Omega-3 fatty acids
Which HMG-CoA reductase inhibitor was recently given a black box warning? What was it?
Doses 80mg or higher may cause rhabdomyolysis.
What is the MOA of bile acid sequestrates/resins? Precautions?
Bind bile acids in the small intestine & are excreted. Other drugs must be taken 1 hr before or 4-6 hrs after bile sequestrants (makes compliance/adherence difficult). May cause deficiency of fat-soluble vitamins A, D, E, K.
What is the indication for fibric acid derivatives? Examples?
Given to pts. with high triglycerides (not given to lower LDL).
Ex: gemfibrozil, fenofibrate, clofibrate
What is the MOA of cholesterol absorption inhibitors? Example?
Inhibits absorption of cholesterol in the small intestine.'
Ex: ezetimibe (Zetia)
How do omega-3 fatty acids help to manage HLD? What must they contain? Can pts. with fish allergy take them?
Lowers triglycerides (little impact on LDL and may actually raise).
Must contain EPA & DHA.
No documented problems in pts. with fish allergy.
How often should LFTs be monitored in patients taking statins? Explain. Describe their use in liver disease.
Measure at initiation and then if symptomatic (changed effective May 2012).
Increase in LFTs is usually transient.
May use in chronic stable liver disease, avoid with acute liver failure & cirrhosis.
What are the treatment goals of angina?
Relieving anginal episodes.
Preventing additional episodes.
Preventing progression of CHD.
Reducing risk of MI.
Improving functional capacity.
What lifestyle changes should be initiated for management of angina?
Low cholesterol, low fat diet.
What drug classes are used for management of angina? What are their MOAs?
ACE & ARBs-block vasoconstriction & aldosterone effects.
Nitrates-control acute attack & used prophylactically-cause dilation throughout vasculature
Beta Blockers-reduce myocardial O2 demand & workload of heart. Good w/ nitrates.
CCBs-cause vasodilation of coronary & peripheral vessels-best with vasospastic angina.
What are adverse effects of nitrates?
headache, flushing, dizziness, weakness, orthostatic hypotension, reflex tachycardia
Avoid using with vasodilators!
What drugs may not be given with organic nitrates?
PDE5 inhibitors (drugs used to treat erectile dysfunction)
Ex: sildenafil (Viagra)
Describe the use of warfarin (Coumadin) in anticoagulation. Indications? INR for A-Fib? Precautions? Antidote?
Warfarin has been mainstay for prevention of clot formation after valve replacement, in A-Fib, post-op in orthopedic sx, etc.
Lowered dose in CHF, malnourished & elderly.
In pregnancy, heparin is preferred due to decreased transfer to fetus.
Vit. K to reverse effects. If INR > 10 hold Coumadin and give Vit K PO.
What are the "New Chest Guidelines" for Antithrombotics? Discuss.
1. Now recommend giving ticagrelor (Brilinta) over clopidogrel (Plavix) with ASA after an ACS. It's more effective than Plavix reduced bleeding risk. Take only 81mg of ASA.
2. Clopidogrel goes generic in the near future & will be much less expensive, plus it is Q day not BID like Brilinta. 3. Prasugrel (Effient) is an alternative to the above but causes more bleeding.
What is the new drug used in place of Coumadin? Advantages? Disadvantages?
Dabigatran (Pradaxa) is a once daily drug that is indicated for thrombus formation in patients with A fib. Benefits of this over warfarin:
Does not undergo metabolism through the CYP450 system (fewer drug interactions).
INR does not need to be monitored.
Superiority in lowering stroke risk.
Problem: No antidote & expensive (even when factoring cost of INR measurements).
What medications are indicated to manage heart failure? MOAs?
Diuretics - reduce edema through reduced blood volume.
Hydralazine (vaso/nitrat) - for preload & afterload reduction.
Inotropic agents - restore organ perfusion & reduce congestion.
Antiplatelets (ASA, Plavix)
Beta blockers - for LVEF improvement & arrhythmia prevention.
ACE/ARBs - for vasodilation & LVEF improvement Digoxin - can cause small increase in cardiac output
What drugs are contraindicated with heart failure?
NSAIDS, CCBs and most antiarrhythmics except for amiodarone and dofetilide.
What classes of drugs are antiarrhythmic? Examples?
Sodium channel blockers - i.e. Rythmol.
Beta blockers - i.e. lopressor
Potassium channel blockers - i.e. cordarone, tikosyn, multaq, corvert, betapace
Calcium channel blockers - i.e. calan & cardizem
Mechanisms of Blood Pressure Control:
Sympathetic nervous system
Works on the heart rate & contractility.
Calcium Channel Blockers
Centrally acting drugs
How do beta blockers work on heart rate & contractility?
With beta-adrenergic stimulation via epinephrine, causes increased stroke volume in the heart muscle. Beta-blockers decrease stroke volume thereby lowering blood pressure.
How do calcium channel blockers work on heart rate & contractility?
They work by blocking the entry of calcium into the myocardial cells or vascular smooth muscle cells, which causes a decrease in contractility, a decrease in heart rate and vasodilation.
How do centrally acting drugs work on heart rate and contractility?
They decrease cardiac output and decrease peripheral resistance: these drugs affect the vasomotor center in the brain by limiting the sympathetic outflow to the heart and blood vessels. Example methyldopa, Alsomet; best used in pregnancy.
Mechanism of Blood Pressure Control:
How do vasodilators work?
The alpha adrenergic receptor blockers cause direct vasodilation. Example: prazoxin, terazosin.
Mechanism of Blood Pressure Control:
Angiotensin Converting Enzymes ACE Inhibitors
Angiotensin Receptor Blockers ARBs
How do diuretics work on vascular volume?
They decrease blood volume & sodium levels. The different types of diuretics are classified by the anatomic site within the kidney tubule they exert their influence on. Example: Thiazides, Loops, & Potassium sparing.
How do ACE Inhibitors work on vascular volume?
These drugs inhibit the conversion of angiotensin 1 into angiotensin II, thereby decreasing arterial pressure.
Cardioselective Antihypertensive Agents
Beta blockers achieve their effects by competing for adrenergic receptor binding sites. Beta 1 receptors predominate in cardiac tissue. Beta 2 receptors predominate in bronchial & vascular smooth muscles, & liver.
Beta 1 have fewer adverse effects such as gluconeogenesis in the liver or bronchial constriction.
Give an example of Beta 1 cardioselective agent.
Beta 1 i.e. Atenolol or tenormin, Metoprolol or lopressor
Give an example of nonselective agent.
Timolol, betim, Propanolol, Inderal.
What are the major actions of Calcium Channel Blockers?
They decrease myocardial contractility, a negative ionatropic force. Slow rate of ventricular contractions, cause coronary artery dilation, peripheral arterial dilation and reduced peripheral resistance. They work by blocking the movement of calcium into the cell membranes of the cardiac & smooth muscle. 2 types DHP, which is the largest group, & NonDHP.
Give examples of DHP, CCBs and differentiate between nonDHP.
Nifedipine, procardia, amlodipin or norvasc are examples. The main difference between DHP & non DHPs is that they do not effect the cardiac conduction system. Therefore they are not used for cardiac arrhythmias.
Give examples of Non DHP
Examples: Verapamil or calan & diltiazem or cardiazem. They are used both for hypertension and arrhythmias.
Key contraindication with CCB & heart failure?
CCBs should NOT be used in pts with heart failure. The major side effect of CCBs is a tendency to cause peripheral edema & reflex tachycardia. A specific population that CCBs are known to work well with is the African American population.
How do potassium sparing diuretics work?
They inhibit sodium re-absorption in the collecting duct, opposite of distal tubule, which spares the potassium depletion that occurs when sodium is not reabsorbed distally.
What is the most serious side effect of potassium sparing diuretics?
Hyperkalemia which is especially dangerous in clients on ACE inhibitors or in diabetes or renal impairment.
How are potassium sparing diuretics primarily used and give an example?
The are used in conjunction with thiazide diuretics to counter act the potassium loss.
Example: spironolactone or aldactone.
What medications are indicated for people with diabetes type 1?
What medications are indicated for people with diabetes type 2?
What medications are indicated for people with heart failure?
ACE inhibitors, diuretics, beta blockers, ARBs, aldosterone receptor antagonists.
What medications are indicated for older adults with isolated systolic hypertension?
Diuretics, CCBs,-long acting DHP.
What medications are indicated for nondiabetic people with renal disease?
What medication are indicated for people after suffering from a myocardial infarction?
Beta blockers-non ISA, ACE inhibitors-when systolic function is present.
What medictions work in favor of people with comorbid angina?
Beta blockers, CCBs
What medication have favorable affect with atrial fib and tachycardia?
Beta blockers, CCBs-non-DHP
What medications work favorably for dyslipidemia?
What medications work favorably fro hyperthyroidism?
What medications work favorably with migraine?
Beta blockers-non cardioselective, CCBs-non DHP
What medications work favorably with myocardial infarction?
Diltiazem and verapamil
What medications work favorably with osteoporosis?
What medications are contraindicated in bronchospastic disease?
What medications are contraindicated in depression?
Beta blockers, alpha antagonists, reserpine
What medications are contraindicated in dibetes types 1 & 2?
Beta blockers, high-dose diuretics.
What medications are contraindicated in dyslipidemia?
Beta blockers-non ISA, high dose diuretics
What medications are contraindicated in gout?
What medications are contraindicated in heart block?
Beta blockers, CCBs-non DHP
What medications are contraindicated in heart failure?
Alpha blockers, CCBs except amlodipine and felodipine.
What medications are contraindicated in peripheral vascular disease?
What medications are contraindicated in pregnancy?
Beta blockers, ACE inhibitors and ARBS
What medications are contraindicated in renal insufficiency?
potassium sparing diuretics, CCBs-especially DHP
What medications are contraindicated in renovascular disease?
ACE inhibitors and ARBs
ACE inhibitors are twice as likely to cause what in women?
CCBs cause more of what in women vs men?
What is more likely to occur to men taking thiazide diuretic?
Thiazides are more likely to cause what electrolyte imbalance in women?
hyponatremia & or hypokalemia.
What medications do not work well in African Americans?
ACE inhibitors and ARBS
What medications have an increased affect on African Americans?
Increased response to thiazide diuretics.
What medications are contraindicated with NSAIDS and why?
ACE & ARBs, can worsen heart failure.
What medicatiosn are teratogenic and contraindicated in pregnancy?
ACE, ARBs, Direct rennin inhibitors DRI's. They are category C in 1st trimester and Cat D in the remainder of pregnancy.
Discuss medications for use in breasfeeding
HCTZ at low dose is safe. some beta blockers but Atenolol and Acebutolol are contraindicated due to extensive excretion in breast milk. Some ACEs are safe in full-term infants, but contra in preterm due to nephrotoxicity. CCBs have low breastmilk levels and safest.
How does our body obtain cholesterol?
Cholesterol can be made endogenously by the liver, or by dietary sources. Cholesterol is essential for the production of steroids, cell membranes and bile acids.
What are the two most common lipids transported in the blood stream?
Triglycerides and cholesterol
What can elevated cholesterol levels lead to?
What can elevated triglycerides lead to?
How do cholesterol and triglycerides become transportable in plasma?
Lipoproteins wrap the cholesterol and triglycerides in a protein coating in order to make the fats water-soluble, thus making them transportable in plasma.
Low-density lipoproteins, the bad guys
These have holes in them that the cholesterol leaks out of. This is of particular concern with narrow, twisted vessels such as those of the heart and brain. They can leak out and get stuck causing a thrombus.
High-density lipoproteins, the good guys
These good guys are smaller, more compact and they tend to accept cholesterol as opposed to giving it up.
Very low desity lipoproteins VLDL
These are the major carrier of endogenous triglycerides. Each VLDL particle contains one molecule of apolipoprptein B-100, which allows transfer of lipid content to cells.
Cholesterol: What is the Adult Treatment Panel III LDL goals & recommendations for High Risk?
High risk CHD or equivalent 10 year risk 20%.
LDL less than 100mg/dl, with optimal goal less than 70.
Initiate lifestyle changes if greater than 100 and consider drug therapy if greater than 100 after life changes.
Cholesterol Moderately High Risk goals & recommendations.
2+ risk factors, 10 year risk 10-20%. LDL goal less than 130, if greater than 130 initiate lifestyle changes, then initiate drug therapy.
What goals & recommendations are there for moderate risk cholesterol level?
Moderate risk is 2+ risk factors 10 year risk less than 10%. LDL goal less than 130, if greater than 130 start lifestyle changes. If greater than 160 consider drug therapy.
What goal and recommendations are there for low risk cholesterol level?
Low risk is 0-1 risk factors. LDL goal less than 160, if greater than 160 start lifestyle changes, if greater than 190 initiate drug therapy.
How do bile acid resins decrease LDL levels?
2nd line RX. They irreversibly bind to bile acids in the gut and prevent their reabsorption. Bile acid resins block the recycling of bile acids in the intestine. To replace the lost bile acids, the liver is forced to remove more cholesterol from the blood to manufacture more bile.
How do HMG-CoA Reductase Inhibitors-statins decrease LDL?
1st line RX. The statins block an enzyme in the cholesterol synthesis pathway. They are contraindicated in pregnancy because pregnant women need cholesterol for fetal growth and development. The antifungals are contraindicated with patients who are taking statins due to drug-drug interaction through the CYP450 system. Often elderly patients who are on statins request an oral antifungal for onychomycosis so it is important to remember that other alternatives for nail fungus should be explored.
How do Fibric acid derivatives lower Triglyceride levels?
3rd line RX. Lopid, gemfibrozil, fenofibrate, tricor. They alter the rate of synthesis of specific lipoproteins. They are used for clients to lower triglyceride levels
How do selective intestinal cholesterol inhibitors work to lower LDL?
3rd line RX. Ezetimibe, currently available alone as Zetia or in fixed combination with zocor as Vytorin. acts at the brush border of the small intestine to inhibit absorption of cholesterol. This results in reduced hepatic cholesterol stores and increased blood clearance. Combination with statins results in a synergistic effect on LDL-C reduction.
How do you manage myopathy side effects of statins?
Up to 30% of people on a statin will complain of muscle pain. If this occurs, check the CK level & if greater than 10 times normal or if symptoms are intolerable for the patient stop the statin. Try to lower the dose, change to fluvastain, pravastatinor low dose rosuvastain. Check drug interactions. Suggest alternate day dosing. Correct low Vit D level and hypothyroidism. CoQ10 100-200mg/d
What are the risk facotrs for hypertriglyceridemia?
Level greater than 200 associated with metabolic syndrome, CVD, genetic predisposition, sedentary lifestyle, DM 2, high CHO intake, smoking and drinking.
How is isolated elevated triglycerides reated?
level greater than 500 with low HDL & normal LDL levels are treated with high dose fish oil containing DHA & EPA and fibrates, such as fenobibrate, clofibrate. Niacin not used as much anymore.
Which 2 hyperlipidemia drugs do you not combine?
Statins and fibrates, due to the combined adverse effects.
What is the recommendation for Omega 3 fatty acid intake for people without CHD?
Eat a variety of oily fish at least twice a week. include oils anfd foods rich in a-linolenic acid, such as flaxseed, canola and soybean oils; flaxseed and walnuts.
What is the recommendation for Omega 3 fatty acid intake for people with documented CHD?
Consume at least 1 gram of EPA DHA per day, preferably from oily fish. Consideration of supplements consulting with provider.
What is the recommendation for Omega 2 fatty acid intake for people needing triglyceride lowering?
2-4 grams of EPA+DHA per day provided as capsules under a providers care.
Describe how coumadin works?
Warfarin inhibits the formation of prothrombin leading to slowed clot formation. Although warfarin is indisputable as an effective method to prevent clot formation, it is a high risk drug, due to its narrow therapeutic range and ability to be altered by certain foods, drugs and even altitude. Also, the patient who is taking warfarin must be able to take their medication regularly and adjust doses accordingly if the INR reveals a deviation from the desired 2.0-3.0. This is particularly problematic in the elderly with dementia as following directions for dosing is essential to prevent hemorrhage or clot formation.
What does warfarin inhibit?
Inhibits the action of Vitamin K which decreases the synthesis of several clotting factors. It has a slow onset and is 99% plamsa bound so it takes time for it to exert its full effects. The high protein binding is responsible for drug-drug interactions.
What does ASA and NSAIDS inhibit?
Aspirin & NSAIDs inhibit platelet aggregation. The effects of NSAIDs on platelet aggregation, as opposed to aspirin, are reversible and last for a shorter period of time, depending on drug half-life. Typically platelet function returns to normal within 24 hours of discontinuation of ibuprofen use in healthy individuals.
What does Plavix inhibit?
What are the indications for plavix?
NSTEMI to decrease rate of cardiovascular death or stroke. For STEMI, it reduces the rate of death from any cause.Dual therapy with ASA, without evidence to support efficacy. It is metabolized thru CYP450 system so poor metabolizers will not get effective benefit. Expensive.
What is Dabigatran or Pradaxa?
A direct thrombin inhibitor, used to reduce stroke and systemic embolism in pts with nonvalvular atrial fib. Works by inhibiting both free & clot-bound thrombin. Works quickly and at a fixed dose.
How is Dabigatran or Pradaxa excreted?
Thru the renal pathway with no involvment of the CYP450 isoenzymes. Very expensive, superior in lowering stroke & emboli than coumadin.
Explain the APN's role in anticoagulation therapy.
APN's often do not initiate anticoagulant therapy in the outpatient setting but are often responsible for monitoring levels and making dosage adjustments
Goal for INR?
What is initial dose of coumadin and how is it monitored?
5-10 mg per day. Checking INR every 3 days until therapeutic, then weekly, then monthly.
When should dosage be lowered with coumadin?
In the elderly, malnourished, liver disease, major surgery and other drugs that impact coumadin levels. Monitor liver function. Coumadin is highly protein bound so watch for drug-drug interactions.
What education should you provide to your patient on coumadin?
herbal therapies; garlic, gingko, vitamin E or increases/decreased consumption of green leafy vegetables. Caution pt about eating broccoli, greens, and other sources high in Vitamin K, have them use an electric razor, no ASA or NSAIDS, monitor for bleeding wear bracelet or card in wallet.
What pregnancy category is heparin?
Does heparin cause fetal harm and is it safe during breastfeeding?
Not usually, due to it's high molecular weight & negative ionic charge, it is unlikely to transfer at significant doses to the placenta. For these reasons it is also safe during breastfeeding.
What pregnancy category is Coumadin?
Can coumadin be used during pregnancy? Explain.
Contraindicated at any point in pregnancy, can cause miscarriage, stillbirth and neonatal death. Most critical time is 6-9 wks gestational age when fetal exposure can cause "fetal warfarin syndrome" including facial deformations, airway obstruction.
Can coumadin be used post partum?
It is often used prophylactically, after 6 weeks post-partum for those with history of thrombosis. It is compatible with breastfeeding. While the risk is low due to high protein binding, and low passage into breast milk, prescribe with caution and observe the infant for petechiae and ecchymoses
How does genetics play a role in warfarin therapy?
Warfarin is one of the most recognized medications for which genetic variation plays an influential role. Enzymatic components CYP450 & CYP2C9 will metabolize it differently in the liver and can be found in 10-20T of Caucasian and African Americans. In 2007, the FDA approved labeling language indicating the use of genetic tests to determine optimal starting doses for individual patients with these genetic variations, who might need lower dosages. While not yet mandatory, such testing helps reduce the risk of bleeding and hemorrhage from a dose that's too high, and blood clots from a dose that's too low.
What health conditions lead to heart failure?
Conditions leading to heart failure are hypertension, CAD, idiopathic cardiomyopathy, MI, PE, and sepsis as well as certain drugs.
The New York Heart Association places heart failure patients into one of four categories depending on symptom. The ACCF/AHA Guidelines were later developed to complement the NYHA Functional Classification. What are the classifications?
Stage A, B, C, & D
Explain Stage A heart failure.
Patients that are high risk for HF and are without structural disease or symptoms- ACEI or ARB started.
Explain Stage B heart failure.
They have structural disease but without S&S of HF
Beta blockers may be added
Implantable defibrillators may be initiated
Explain Stage C heart failure.
Structural disease with prior or current symptoms of HF
Diuretics added to ACEI & beta blockers
Also aldosterone antagonists, ARBs, digital, hydralazine/nitrates
Explain Stage D heart failure.
Refractory HF that requires specialized interventions
1. Decision as to level of care at this point
2. " Extraordinary measures"- heart transplant, chronic inotropes, other drugs
What is the goal to pharmacotherapy of heart failure?
To prevent complications, increase survival, & reduce symptoms. Medications that are used in the management of heart failure are ACE inhibitors, diuretics, digoxin, beta blockers & vasodilators in patients who do not tolerate ACE inhibitors. Medications that should be avoided are nonsteroidals (NSAIDs), antiarrhythmics and CCBs.
What are the common causes of arrhythmias?
They are a result of either an abnormality in the generation of the impulse, a conduction problem or a combination of both. The abnormalities in impulse generation are either automatic or a result of some type of trigger. The abnormal automaticity most likely occurs due to a lowered resting membrane potential. The abnormal triggers occur during phase II , III or IV of the action potential. Conduction issues are most commonly caused by a block or reentry, the most common cause of arrhythmias. Conduction issues caused by blocks or re-entry issues.
What are the therapy goals of antiarrhythmics?
Relieve irregular rhythm
Establish sinus rhythm
Prevent additional episodes of arrhythmia
What are the actions of antiarrhythmic drugs?
All antiarrhythmics alter membrane ion conduction
Decrease or increase conduction velocity
Alter excitability of cardiac cells by changing duration of refractory period
Suppress abnormal automaticity.
How do you choose which antiarrhythmic to use?
The specific arrhythmia
Overall risk to health
Underlying structural heart disease
Symptoms experienced by the patient.
Amiodarone is what class of antiarrythmic?
What are the potential side effects of amiodarone that you will need to teach your patient about?
Hypothyroidism due to high iodine content of the drug- monitor TSH
* Pulmonary toxicity- both as an acute reaction and pulmonary fibrosis development
Hepatotoxicity- monitor LFTS
Reversible slate blue color of the skin
Photosensitivity - patients should be advised to use sunblock
Corneal deposits (do not effect vision) and rarely optic neuritis
*Pulmonary toxicity is the most lethal of side effects
How are antiarrhythmics classified?
Class 1, which has 3 sub classes 1a, 1b, 1c,
Class II, III and IV
What are class 1 antiarrhythmics? Give examples.
Sodium Channel Blockers
1a intermediate onset; quinidine, procinamide, norpace,
1b fast onset; lidocaine, mexiletine, phenytoin-dilantin
1c slow onset; flecainide, propafenone-rythmol
What are class II antiarrythmics? Give examples.
Examples; atenolol, metoprolol, esmolol, propranolol
What are class III antiarrythmics? Give examples.
Potassium Channel Blockers
Examples: amiodarone, dofetilide-tikosyn, dronedarone-multaq, ibutilide-covert, sotalol-betapace
What are class IV antiarrythmics? Give examples.
Calcium Channel Blockers
Examples; diltiazem-cardiazem, verapamil-calan
What medication is the foundation of angina therapy & how do they work?
Nitrates act by relaxing smooth muscle, which leads to vascular dilation. Nitrates may also decrease myocardial oxygen demand by reducing both left ventricular filling pressure, pre-load, and end-diastolic volume.
Discuss dosage and handling of short acting nitroglycerin.
Clients with angina should have access to short-acting nitroglycerine at all times. A dose of 0.3-0.4 may be repeated up to 3 times at 5-minute intervals in acute attacks. Medication must be kept in original tightly capped amber vial and it must be with the client. Clients should replace the nitroglycerine at least every 6 months.
How do beta blockers help in treating angina?
They decrease myocardial oxygen consumption by reducing contractility, blood pressure, and heart rate. Beta-blockers have been found to prolong life in clients who have had MIs. They are also helpful for clients with exercise-induced angina
How do calcium channel blockers work in the treatment of angina?
By blocking the influx of calcium through slow channels into vascular smooth muscle & myocardial cells. This promotes arterial vasodilation, which decreases oxygen demand by decreasing afterload. They also decrease coronary vasospasm, improve collateral flow, decrease contractility and enhance diastolic relaxation of the left ventricle, which increases coronary perfusion. Although calcium channel blockers relieve symptoms and provide many of the physiological changes appropriate for the relief of angina they have not clearly been shown to reduce morbidity or mortality.
What is the mechanisms of adrenergic receptor activation?
AKA sympathomimetics, Because their effects mimic those caused by the sympathetic nervous system. Most adrenergic agonists act by direct activation of adrenergic receptors. A few act by indirect mechanisms: promotion of norepinephrine release, blockade of norepinephrine uptake, and inhibition of norepinephrine breakdown.
What are the 2 chemical classes of adrenergic agonists?
Catecholamines which can't be taken orally cannot cross blood brain barrier
Non-catecholamines-can take PO, longer duration & can cross blood brain barrier
What are the clinical consequences of Alpha 1 Activation?
Activation of alpha1 receptors causes vasoconstriction and mydriasis.
Alpha1 agonists are used for hemostasis, nasal decongestion, and elevation of blood pressure, and as adjuncts to local anesthetics.
What are the adverse effects of Alpha 1 Activation?
Major adverse effects that can result from alpha1 activation are hypertension and local necrosis if infiltration occurs.
What are the clinical consequences of Alpha 2 Activation?
Activation of alpha2 receptors in the periphery is of minimal clinical significance. In contrast, drugs that activate alpha2 receptors in the central nervous system produce useful effects
What are the clinical consequences of Beta 1 activation?
All of the clinically relevant responses to activation of beta1 receptors result from activating beta1 receptors in the heart.
Activation of cardiac beta1 receptors increases heart rate, force of contraction, and conduction through the AV node.
Drugs that activate beta1 receptors can be used to treat heart failure, AV block, and cardiac arrest
What are the adverse effects of Beta 1 activation?
Potential adverse effects from beta1 activation are tachycardia, dysrhythmias, and angina
What are the clinical consequences of Beta 1 activation?
Drugs that activate beta2 receptors are used to treat asthma and delay preterm labor.
What are the adverse effects of Beta 2 acivation?
Principal adverse effects from beta2 activation are hyperglycemia, mainly in diabetic patients, and tremor.
How do diuretics work?
Most diuretics block active re-absorption of sodium & chloride, & prevent passive re-absorption of water. the amount of diuresis is directly related to the amount of sodium and chloride re-absorption blocked. Drugs that act early in the nephron are in a position to block the most amount of solute re-absorption, & produces the most diuresis.
What is an example of 'High-ceiling diuretic and how do they work?
Loop diuretics, Lasix block sodium and chloride reabsorption in the loop of Henle.
High-ceiling diuretics produce the greatest diuresis.
In contrast to thiazide diuretics, high-ceiling diuretics are effective even when the glomerular filtration rate is low.
What are the adverse effects of high-ceiling diuretics? (Loop)
Dehydration through excessive fluid loss.
Hypotension by decreasing blood volume & relaxing venous smooth muscle.
Hearing loss, which is usually reversible.
Hypokalemia caused by high-ceiling diuretics is a special problem for patients taking digoxin.
What are high ceiling diuretices & thiazides used to treat?
Hypertension, edema associated with heart failure, cirrhosis, and kidney disease.
Are thiazide diuretics as effective as high ceiling diuretics? give an example.
No, they are less effective and are ineffective when glomerular filtration rate is low.Example; Hydrochlorothiazide
What are adverse effects of thiazides?
dehydration, hypokalemia which is a special problem with patients taking digoxin. Hearing loss does not occur with thiazides.
Give an example of a potassium sparing diuretic and how it works.
Example; Spironolactone & triamterene, which acts by directly or indirectly blocking sodium-potassium "exchange" in the distal convoluted tubule causing only modest diuresis. Used primarily to counteract potassium loss in patients taking high-ceiling diuretics or thiazides.
What are the adverse effects of potassium sparing diuretics, including drug interactions?
The principal adverse effect of potassium-sparing diuretics is hyperkalemia.
Because of the risk of hyperkalemia, potassium-sparing diuretics should not be combined with one another or with potassium supplements, and they should be used cautiously in patients taking ACE inhibitors, angiotensin-receptor blockers, or direct renin inhibitors
Antidiuretic Hormone AKA Vasopressin
Synthesized by hypothalmus, then neurons secreted by posterior pituitary. ADH counter-acts our ability to excrete H2O. Target tissue=kidneys & vascular smooth muscle. Results=stimulates retention of H2o in kidneys, vascular smooth muscle contract, increase total peripheral resistance TPR, resulting in increased BP
Stimulates secretion of ADH, increase thirst, & Increased peripheral resistance = volume expansion
What is afterload?
The pressure the heart must over-come to push the blood out to the rest of the body. i.e. mean arterial pressure MAP.
Another way to look at it is the load against which a muscle exerts its force. For the heart, afterload is the AP that the left ventricle must overcome to eject blood.
What is pre-load?
Preload is the amount of blood sitting in the heart right before it contracts. i.e end diastolic pressure.
Another way to look at it is the amount of tension stretch, applied to a muscle prior to contraction. In the heart, preload is determined by the force of venous return.
What is cardiac output?
Stroke volume-the amount of blood ejected per beat, times heart rate
CO=SV x HR
What is stroke volume?
Determined by myocardial contractility, cardiac pre-load, & cardiac afterload.
How is arterial pressure regulated?
By the autonomic nervous system, the renin-angiotensin-aldosterone system, the kidneys, & natriuretic peptides.
What causes reflex tachycardia?
Drugs that lower arterial pressure, trigger the baroreceptor reflex which causes reflex tachycardia. Therefore the baroreceptor reflex can temporarily negate efforts to lower AP with drugs. Use of BB suppresses reflex tachycardia.
How does the RAAS support arterial pressure?
By constriction of the arterioles & veins.
Retention of water by the kidneys. Vasoconstriction is mediated by angiotensin II; water retention is mediated in part by aldosterone.
What causes orthostatic hypotension?
Decreased venous return secondary to pooling of blood in veins, which can occur as we stand up.
How does the RAAS Renin Angiotensin Aldosterone System work?
The RAAS helps regulate blood pressure, blood volume, and fluid and electrolyte balance. The system can mediate cardiovascular pathology.
It acts through production of angiotensin II and aldosterone.
What are the actions of angiotensin II?
Angiotensin II has much greater biologic activity than angiotensin I or III.
Angiotensin II is formed by the actions of two enzymes: renin and ACE.
It causes vasoconstriction, primarily in arterioles, & release of aldosterone. In addition, angiotensin II can promote pathologic changes in the heart and blood vessels
Explain the actions of aldosterone.
Aldosterone acts on the kidneys to promote retention of sodium & water. It can also mediate pathologic changes in cardiovascular function.
What do the beneficial effects of ACE inhibitors reult from?
The inhibition of Ace & kinase II, the name for ACE when the substrate is bradykinin. This decreases production of angiotensin II, which causes vasodilation, decreased blood volume, & prevention or reversal of pathologic changes in the heart & vessels mediated by angiotensin II & aldosterone.
What causes the "first dose" hypotension using ACE inhibitors?
A severe drop in circulating angiotensin II.
What causes the 'noxious cough' associated with ACE inhibitors?
The cough is secondary to accumulation of bradykinin, this is the most common reason for discontinuing use of ACE inhibitors.
Are ACE inhibitors safe during pregnancy? Why?
No. It can cause major fetal malformations, & should be avoided during pregnancy. Until recently, we thought that risk was limited to exposure during the second and third trimesters. However, new data indicate that exposure during the first trimester may also be dangerous as well.
What is Aliskiren?
A DRI-direct renin inhibitor that binds tightly with renin and inhibits cleavage of angiotensinogen into angiotensin I. As a result the drug suppresses the entire RAAS.
How does Aliskiren, a DRI- direct renin inhibitor, work?
Like the ACE & ARBS, aliskiren causes vasodilation, suppresses aldosterone release, promotes excretion of sodium and water, reduces blood pressure, and causes birth defects and angioedema. These drugs are not interchangeable.
What effect does CCB have on the heart?
In the heart, calcium entry increases heart rate, atrioventricular, AV conduction, and myocardial contractility, and hence calcium channel blockade has the opposite effects. All CCBs promote vasodilation, and are useful in hypertension and angina pectoris.
What are some adverse effects verapamil and diltiazem cause?
Because of their cardiosuppressant effects, verapamil and diltiazem can cause bradycardia, partial or complete AV block, and exacerbation of heart failure. BBs intensify cardiosuppression caused by both drugs.
What is the definition of primary-essential hypertension?
HTN with no identifiable cause. This is the most common cause of HTN.
Review of BP control.
The baroreceptor reflex, the kidneys, and the renin-angiotensin-aldosterone system (RAAS) can oppose our attempts to lower BP with drugs. We can counteract the baroreceptor reflex with a beta blocker, the kidneys with a diuretic, and the RAAS with an angiotensin-converting enzyme (ACE) inhibitor, angiotensin II receptor blocker (ARB), direct renin inhibitor (DRI), or aldosterone antagonist.
What is the major cause of antihypertension treatment failure?
Lack of patient adherence due to; no symptoms so drug benefits aren't obvious. HTN progresses slow, so pts thing they can postpone tx. Tx is complex & expensive, lifelong & adverse effects.
What is the most common complication of pregnancy?
When do you start to screen for total cholesterol, LDL, HDL cholesterol & triglycerides?
At age of 20, then every 5 years.
Which statins are metabolized by CYP3A4?
atrovastatin, lovastatin & simvastatin. Their levels can be increased by CYP3A4 inhibitors such as cyclosporine & erythromycin, ketoconazole & ritonavir.
What do you monitor for a patient taking statin complains of muscle pain?
CK, creatine kinase, check for myopathy. Rhabdo
Give an example of bile-acid sequestrant.
These drugs are not absorbed from the GI tract, so they do not cause systemic adverse effects.
Arterial thrombi are best prevented by use of what type of drug?
Antiplatelet drugs...ASA, plavix
Venous thrombi are best prevented by use of what type of drug?
Anticoagulants, coumadin, heparin.
Name direct thrombin inhibitors
Bivalirudin, lepirudin, argatroban, desirudin, dabigatran
Why do you take a patients nitro patch off at night?
To prevent tolerance, allow at least 8 hrs of being drug free per day, when using long duration nitro.
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